•  
  •  
 

DOI

https://doi.org/10.1016/j.jds.2025.10.039

First Page

562

Last Page

569

Abstract

Background/purpose Human papillomavirus (HPV)-positive oropharyngeal cancer (OPC) generally shows better outcomes, yet a subset of patients develops aggressive lymphatic metastasis. The molecular determinants of this divergence remain unclear. This study explored the apolipoprotein B mRNA editing enzyme catalytic subunit 3B (APOBEC3B)/anti-silencing function 1B histone chaperone (ASF1B) axis as a potential mediator linking human papillomavirus (HPV) infection, DNA damage, and transforming growth factor beta (TGF-β) signaling in OPC. Materials and methods Transcriptomic and clinical datasets from The Cancer Genome Atlas (TCGA) were analyzed to examine correlations among APOBEC3B/ASF1B expression, HPV status, and TGF-β signaling activity. Functional assays using HPV-positive and HPV-negative cell models assessed APOBEC3B/ASF1B expression, replication protein A2 (RPA2) activation, and epithelial–mesenchymal transition (EMT) markers through quantitative polymerase chain reaction (qPCR), western blotting, and immunofluorescence. Results HPV infection markedly enhanced APOBEC3B and ASF1B expression, accompanied by RPA2 upregulation and EMT features. Silencing APOBEC3B reduced RPA2 and ASF1B levels and suppressed TGF-β signaling. Conclusion These findings identify APOBEC3B/ASF1B as a central pathway through which HPV infection activates TGF-β signaling and promotes EMT, offering potential biomarkers and therapeutic targets for high-risk HPV-positive OPC.

Publication Date

1-1-2026

Share

COinS